Thyroid storm is a severe form of thyrotoxicosis, where a sudden spike in thyroid hormones accelerates metabolism and disrupts multiple organ systems. It is often triggered by stressors like surgery or infections, overwhelming the body's ability to cope. Moreover, thyroid storm can increase the body's sensitivity to catecholamines, exacerbating the hypermetabolic state and leading to organ dysfunction. Some patients exhibit clinical symptoms like high fever, excessive sweating, and rapid heartbeat, linked to heightened catecholamine activity. Globally, the incidence of thyroid crisis among hospitalized patients is approximately 0.2–5.6 per 100,000 per year (1, 2). Individuals diagnosed with hyperthyroidism, whether undergoing thyroid or non-thyroid surgical procedures, are susceptible to thyroid storm during the perioperative period. Reports of intraoperative and postoperative thyroid storm in non-thyroid surgeries are scarce. This rarity is primarily attributed to the prevalent use of antithyroid medications to achieve a euthyroid state preoperatively. Thyroid storm can progress to heart failure, atrial fibrillation, and liver dysfunction (3). If not promptly diagnosed and treated, the mortality rate of thyroid storm can be as high as 8%–25% (4).

In this case study, the patient presented with a confirmed preoperative diagnosis of hyperthyroidism and subsequently exhibited prodromal symptoms indicative of a thyroid storm during the postoperative recovery period following right femoral fixation surgery, manifesting as delayed emergence from anesthesia (≥60 minutes) with tachycardia and unresponsiveness The condition was promptly identified, and emergency management protocols were initiated. Furthermore, a comprehensive review of the literature pertaining to the diagnosis and management of perioperative thyroid storm was conducted. We also reviewed existing literature to highlight diagnostic and management principles applicable to similar cases.

We performed a systematic review of the PubMed/Medline database, covering the period from 2005 to 2025, employing the keywords “thyroid crisis” OR “thyroid storm” in conjunction with “perioperative,” “surgery,” “non-thyroid surgery,” or “nonthyroid surgery” using Boolean operators: (thyroid crisis OR thyroid storm) AND (perioperative OR surgery OR non-thyroid surgery). Initially, 211 publications were screened, of which 18 cases satisfied the inclusion criteria for peer-reviewed reports documenting intraoperative or postoperative thyroid storm during non-thyroid surgeries (Table 4). This review was conducted in accordance with the PRISMA guidelines. The surgical procedures included abdominal (n = 5), orthopedic (n = 4), cardiothoracic (n = 4), obstetric (n = 3), and other procedures (n = 2). In this cohort, thyroid storm was observed intraoperatively in 8 patients and postoperatively in 10 patients. Concerning the correlation with pre-existing thyroid conditions, 5 patients had a documented history of thyroid disorders, while 3 patients had documented thyroid symptoms preoperatively but lacked formal diagnosis, suggesting potential oversight in preoperative assessment. Additionally, 8 patients were unaware of any underlying thyroid conditions before undergoing surgery. The most prevalent clinical manifestations included tachycardia (100%, 18/18), fever (56%, 10/18), central nervous system symptoms (27%, 5/18), and heart failure (16%, 3/18). Diagnosis was primarily reliant on thyroid hormone assays and the Burch-Wartofsky Point Scale, with initial evaluations largely guided by clinical presentation. The majority of patients exhibited favorable responses to treatment with antithyroid medications, corticosteroids, and adjunctive supportive therapies. Notably, overall prognosis was favorable, with only one reported mortality due to a postoperative pulmonary complication.

This case illustrates the diagnostic complexity of thyroid storm in postoperative settings, where anesthesia-related confounders (e.g., delayed emergence, hemodynamic fluctuations) may mimic or mask classic features. Unlike typical presentations with hyperthermia and overt hypermetabolism (1), our patient exhibited only tachycardia and altered consciousness, underscoring the need for heightened vigilance in non-thyroid surgeries. Crucially, our patient did not have a fever and had normal FT4 levels, making diagnosis under anesthesia challenging. The patient's anti-thyrotropin receptor antibody (Anti-TSHR) level was 1.32 IU/L, within the normal range (0–1.75 IU/L), reducing the likelihood of Graves’ disease. However, thyroid ultrasound revealed hypoechoic nodules classified as C-TIRADS 4a, suggesting toxic nodular goiter as the probable underlying cause of hyperthyroidism.

Numerous precipitating factors can lead to a perioperative thyroid storm, with its primary clinical manifestations exhibiting considerable variability. These manifestations may impact the central nervous system, cardiovascular system, digestive system, and thermoregulatory processes, as outlined in Table 5 (5). During episodes of acute stress, there is an enhanced cellular response to thyroid hormones. An increase or abrupt release of free hormones results in an amplified response to catecholamines. A rapid increase in thyroid hormone levels, rather than their absolute amounts, is believed to trigger a thyroid storm. Although a trigger is usually needed for a thyroid storm in hyperthyroidism and thyrotoxicosis, up to 30% of cases occur without an identifiable cause.

Thyroid storm diagnosis primarily depends on clinical criteria, with tools like the Burch-Wartofsky Point Scale and Japan Thyroid Association guidelines commonly employed. These methods, however, have limitations, including reduced sensitivity for mild cases and challenges in differentiating thyroid storm from other critical conditions. Additionally, reliance on subjective clinical judgment can lead to variability among healthcare professionals (6). Predicting thyroid storm involves assessing clinical symptoms alongside the Burch-Wartofsky Point Scale, as detailed in Table 1 (3). A score of 45 or greater is highly suggestive of thyroid storm, a score of 25–44 is suggestive of impending storm, and a score below 25 is unlikely to represent thyroid storm. Key clinical signs include hyperthermia, tachycardia, central nervous system disturbances, and gastrointestinal or hepatic dysfunction. Patients may exhibit symptoms such as high fever (temperature >39°C), tachycardia (heart rate >140 bpm), altered consciousness, diarrhea, jaundice, and abnormal thyroid function tests (e.g., decreased TSH, elevated free T3 and T4) (1).Nonetheless, atypical presentations complicate the diagnostic process, as certain patients may initially exhibit acute abdominal symptoms, resulting in potential misdiagnosis. Concurrently, others may experience a thyroid storm alongside other conditions, such as subacute thyroiditis or subarachnoid hemorrhage, further complicating accurate diagnosis (7, 8). Additionally, under anesthesia, some clinical indicators from the Burch-Wartofsky Point Scale may be obscured. In response to these challenges, the Japan Thyroid Association introduced diagnostic criteria in 2012, as detailed in Table 2 (9). Grade 1 indicates a definite thyroid storm and Grade 2 a suspected thyroid storm. Cases are excluded if other underlying diseases clearly cause any of the following symptoms: fever (e.g., pneumonia and malignant hyperthermia), impaired consciousness (e.g., psychiatric disorders and cerebrovascular disease), heart failure (e.g., acute myocardial infarction), and liver disorders (e.g., viral hepatitis and acute liver failure). Therefore, it is difficult to determine whether the symptom is caused by a thyroid storm or is simply a manifestation of an underlying disease; the symptom should be regarded as being due to a thyroid storm that is caused by these precipitating factors (34). Consequently, it is advisable to employ both scoring systems when evaluating patients suspected of experiencing a thyroid storm to enhance diagnostic precision.

Delayed emergence from anesthesia is a multifaceted issue attributable to various factors. It is primarily attributed to the residual effects of anesthetic and analgesic agents, whose metabolism and clearance rates vary among individuals, leading to prolonged awakening times (10). Additionally, less common causes such as cerebral edema or unexpected cerebral venous sinus thrombosis, which may not be immediately evident postoperatively, can significantly impede recovery (11). Neurocognitive recovery delays are particularly concerning in elderly patients and may be associated with the type of anesthetic used, pre-existing conditions like diabetes or prior cerebrovascular events, and intraoperative factors such as hypothermia (12). Moreover, mental health status plays a role, with evidence indicating that patients with pre-existing depression are more susceptible to delayed recovery, potentially due to depression's negative impact on physiological recuperation (13). Thus, delayed emergence from anesthesia results from an interplay of pharmacological, physiological, and psychological factors.

In our case, the potential causes of delayed emergence from anesthesia, such as residual anesthetic agents or metabolic disturbances (including hypoglycemia and electrolyte imbalances), were considered. However, an arterial blood gas analysis was not performed in the post-anesthesia care unit (PACU), representing a significant oversight. Future protocols ought to integrate arterial blood gas (ABG) analysis to facilitate a comprehensive evaluation of delayed emergence and metabolic disturbances, particularly in patients who demonstrate abrupt alterations in consciousness following surgery. This omission hindered the exclusion of carbon dioxide accumulation, electrolyte imbalances, or other potential causes for the delayed emergence. Nevertheless, based on the patient's symptoms at the time, the Burch-Wartofsky Point Scale was calculated as follows: tachycardia (144 beats/min, 25 points), altered mental status (20 points), and absence of fever (0 points), resulting in a total score of 45 points, which strongly indicates a thyroid storm. According to the criteria set by the Japan Thyroid Association, the presence of thyrotoxicosis accompanied by central nervous system disturbance and tachycardia qualified the patient for a grade 1 diagnosis. As a result, a thyroid storm was suspected, and treatment with hydrocortisone and esmolol was given following American and Japan Thyroid Association guidelines (9, 14). Due to the altered mental status and concerns about oral absorption, methimazole was not administered immediately postoperatively. The patient's rapid response to hydrocortisone and esmolol, and subsequent quick awakening, further confirmed the diagnosis of thyroid storm.

Elective surgeries should be postponed for hyperthyroid patients showing symptoms like tachycardia, altered consciousness, fever, and gastrointestinal issues, which indicate a higher risk of thyroid storm. The attainment of a euthyroid state may require a duration ranging from 6 weeks to 18 months and should be managed under the supervision of an endocrinologist (9, 14). The most effective preoperative prophylactic treatment for hyperthyroid patients preparing for surgery involves a comprehensive approach: reducing thyroid hormone synthesis and secretion through the use of thionamides, iodine solutions, or both; safeguarding the cardiovascular system and maintaining hemodynamic stability with beta-blockers; and decreasing circulating free T3 levels while substituting cortisol in patients with adrenal insufficiency through the administration of corticosteroids. In a systematic review on the risk of perioperative thyroid storm conducted by Nikki et al. (4), it was observed that thyroid storms may occur intraoperatively or postoperatively, irrespective of the use of single-drug or combination therapies in the preoperative phase. Notably, this risk is present in both euthyroid and hyperthyroid patients. When selecting an anesthetic strategy, regional anesthesia and peripheral nerve blocks are preferred over general anesthesia whenever feasible. In cases where regional anesthesia techniques are not applicable to the surgical procedure, general anesthesia should be administered with strategies to mitigate intubation responses, ensure adequate analgesia and deep anesthesia, and facilitate smooth extubation (15).

The patient's incomplete adherence to methimazole reflect a critical gap in perioperative optimization. Current guidelines emphasize achieving euthyroidism before elective surgery (9, 14), yet this case demonstrates how subclinical hyperthyroidism (evidenced by normal FT4 but suppressed TSH) can still precipitate storm under surgical stress. Notably, the omission of antithyroid drugs on the day of surgery may have exacerbated hormone release, highlighting the need for strict medication compliance protocols.

According to the treatment guidelines established by the American and the Japan Thyroid Association (9, 14), the management protocol for thyroid storm during and post-surgery encompasses several key interventions. Seizure-like symptoms are treated with diazepam (0.15–0.2 mg/kg, max 10 mg) or propofol (1–2 mg/kg). Fever should be managed with physical cooling methods, avoiding NSAIDs due to their risk of increasing free thyroid hormone release. To inhibit thyroid hormone synthesis, oral propylthiouracil (PTU) is given with a loading dose of 500–1,000 mg, then 200–250 mg every 4 hours, while methimazole can be used orally (60 mg) or intravenously (30 mg daily). One hour after thionamides, iodine agents like Lugol's solution or iopanoic acid are administered to block hormone release. Beta-blockade is achieved with intravenous esmolol (1 mg/kg bolus, then 150 mcg/kg/min infusion) to maintain heart rate under 130 bpm; propranolol or metoprolol are alternatives. To inhibit peripheral T4 to T3 conversion, hydrocortisone (300 mg loading, then 100 mg IV every 8 hours) or dexamethasone (8 mg IV daily) is used. For atrial fibrillation, digoxin is dosed at a total loading of 8–12 mcg/kg titrated over 12 hours, and amiodarone is given if left ventricular dysfunction is present (150 mg over 10 minutes, then 1 mg/min for 6 hours, followed by 0.5 mg/min, max 2.4 g/day). Acute heart failure is managed with IV furosemide (0.5–1 mg/kg), and cardiogenic shock may require dobutamine (2.5–10 mcg/kg/min) and norepinephrine (0.03–0.3 mcg/kg/min) infusions.

While thyroid storm is well-documented in thyroidectomies (4), its occurrence after orthopedic surgery is rare. This case suggests that even minor surgical trauma can trigger storm in poorly controlled hyperthyroidism, particularly when cardiovascular stressors (e.g., pain, fluid shifts) are present. We recommend the implementation of mandatory preoperative endocrine consultations for all patients with hyperthyroidism who are scheduled to undergo non-thyroid surgical procedures, irrespective of their biochemical stability. Such consultations could potentially prevent the omission of necessary medications and ensure optimal thyroid function prior to surgery.

This case highlights the crucial impact of perioperative medication adherence—omission of antithyroid drugs on the day of surgery likely precipitated the storm. Notably, the absence of hyperthermia highlights the risk of missed or delayed diagnosis when relying solely on classic signs. Our experience underscores the need for heightened vigilance and suggests that monitoring protocols for hyperthyroid patients undergoing any surgery should be standardized and multidisciplinary.

Key lessons from this case emphasize the importance of comprehensive perioperative management in patients with hyperthyroidism. Achieving a euthyroid state with antithyroid drugs and beta-blockers before surgery is crucial to prevent thyroid storm, with input from endocrinology being essential. During and after surgery, careful monitoring is necessary as these patients are still at risk, even in non-thyroid procedures. Anesthetic techniques should aim to minimize sympathetic stimulation and hemodynamic instability. Quick diagnosis using the Burch-Wartofsky Scale and Japan Thyroid Association criteria, along with immediate treatment with beta-blockers, corticosteroids, and antithyroid medications, is critical for survival. Educating patients on medication adherence and early symptom detection is also key to avoiding recurrence.

This case adds to the limited literature on thyroid storm triggered by non-thyroid surgeries and reinforces the need for standardized perioperative protocols. Future research should focus on developing risk stratification tools and evaluating anesthetic strategies tailored for hyperthyroid patients across various surgical settings.